ORIGINAL PAPER

Abstract Bone as most of living tissues is able, during its entire lifetime, to adapt its internal microstructure and subsequently its associated mechanical properties to its specific mechanical and physiological environment in a process commonly known as bone remodelling. Bone is therefore continuously renewed and microdamage, accumulated by fatigue or creep, is removed minimizing the risk of fracture. Nevertheless, bone is not always able to repair itself completely. Actually, if bone repairing function is slower than microdamage accumulation, a type of bone fracture, usually known as ‘‘stress frac-ture’’, can finally evolve. In this paper, we propose a bone remodelling continuous model able to simulate microdamage growth and repair in a coupled way and able therefore to predict the occurrence of ‘‘stress frac-tures’’. The biological bone remodelling process is modelled in terms of equations that describe the activity of basic multicellular units. The predicted results show a good correspondence with experimental and clinical data. For example, in disuse, bone porosity increases until an equilibrium situation is achieved. In overload-ing, bone porosity decreases unless the damage rate is so high that causes resorption or ‘‘stress fracture’’.